Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation

Abstract Microglia are integral mediators of innate immunity within the mammalian central nervous system. Typical microglial responses are transient, intending to restore homeostasis by orchestrating the removal of pathogens and debris and the regeneration of damaged neurons. However, prolonged and...

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Autores principales:	Erskine Chu, Richelle Mychasiuk, Margaret L. Hibbs, Bridgette D. Semple
Formato:	article
Lenguaje:	EN
Publicado:	BMC 2021
Materias:	Neurodegenerative diseases PI3K AKT Cell signaling Innate immune system Glia Neurology. Diseases of the nervous system RC346-429
Acceso en línea:	https://doaj.org/article/66e416b4e60b47ce875018a43baf08b7
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spelling	oai:doaj.org-article:66e416b4e60b47ce875018a43baf08b72021-11-28T12:37:40ZDysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation10.1186/s12974-021-02325-61742-2094https://doaj.org/article/66e416b4e60b47ce875018a43baf08b72021-11-01T00:00:00Zhttps://doi.org/10.1186/s12974-021-02325-6https://doaj.org/toc/1742-2094Abstract Microglia are integral mediators of innate immunity within the mammalian central nervous system. Typical microglial responses are transient, intending to restore homeostasis by orchestrating the removal of pathogens and debris and the regeneration of damaged neurons. However, prolonged and persistent microglial activation can drive chronic neuroinflammation and is associated with neurodegenerative disease. Recent evidence has revealed that abnormalities in microglial signaling pathways involving phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) may contribute to altered microglial activity and exacerbated neuroimmune responses. In this scoping review, the known and suspected roles of PI3K-AKT signaling in microglia, both during health and pathological states, will be examined, and the key microglial receptors that induce PI3K-AKT signaling in microglia will be described. Since aberrant signaling is correlated with neurodegenerative disease onset, the relationship between maladapted PI3K-AKT signaling and the development of neurodegenerative disease will also be explored. Finally, studies in which microglial PI3K-AKT signaling has been modulated will be highlighted, as this may prove to be a promising therapeutic approach for the future treatment of a range of neuroinflammatory conditions.Erskine ChuRichelle MychasiukMargaret L. HibbsBridgette D. SempleBMCarticleNeurodegenerative diseasesPI3KAKTCell signalingInnate immune systemGliaNeurology. Diseases of the nervous systemRC346-429ENJournal of Neuroinflammation, Vol 18, Iss 1, Pp 1-17 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Neurodegenerative diseases PI3K AKT Cell signaling Innate immune system Glia Neurology. Diseases of the nervous system RC346-429
spellingShingle	Neurodegenerative diseases PI3K AKT Cell signaling Innate immune system Glia Neurology. Diseases of the nervous system RC346-429 Erskine Chu Richelle Mychasiuk Margaret L. Hibbs Bridgette D. Semple Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
description	Abstract Microglia are integral mediators of innate immunity within the mammalian central nervous system. Typical microglial responses are transient, intending to restore homeostasis by orchestrating the removal of pathogens and debris and the regeneration of damaged neurons. However, prolonged and persistent microglial activation can drive chronic neuroinflammation and is associated with neurodegenerative disease. Recent evidence has revealed that abnormalities in microglial signaling pathways involving phosphatidylinositol 3-kinase (PI3K) and protein kinase B (AKT) may contribute to altered microglial activity and exacerbated neuroimmune responses. In this scoping review, the known and suspected roles of PI3K-AKT signaling in microglia, both during health and pathological states, will be examined, and the key microglial receptors that induce PI3K-AKT signaling in microglia will be described. Since aberrant signaling is correlated with neurodegenerative disease onset, the relationship between maladapted PI3K-AKT signaling and the development of neurodegenerative disease will also be explored. Finally, studies in which microglial PI3K-AKT signaling has been modulated will be highlighted, as this may prove to be a promising therapeutic approach for the future treatment of a range of neuroinflammatory conditions.
format	article
author	Erskine Chu Richelle Mychasiuk Margaret L. Hibbs Bridgette D. Semple
author_facet	Erskine Chu Richelle Mychasiuk Margaret L. Hibbs Bridgette D. Semple
author_sort	Erskine Chu
title	Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
title_short	Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
title_full	Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
title_fullStr	Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
title_full_unstemmed	Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
title_sort	dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation
publisher	BMC
publishDate	2021
url	https://doaj.org/article/66e416b4e60b47ce875018a43baf08b7
work_keys_str_mv	AT erskinechu dysregulatedphosphoinositide3kinasesignalinginmicrogliashapingchronicneuroinflammation AT richellemychasiuk dysregulatedphosphoinositide3kinasesignalinginmicrogliashapingchronicneuroinflammation AT margaretlhibbs dysregulatedphosphoinositide3kinasesignalinginmicrogliashapingchronicneuroinflammation AT bridgettedsemple dysregulatedphosphoinositide3kinasesignalinginmicrogliashapingchronicneuroinflammation
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Dysregulated phosphoinositide 3-kinase signaling in microglia: shaping chronic neuroinflammation

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